Propofol inhibits burn injury-induced oxidative stress injury through SOD2 up-regulation in human dermal microvascular endothelial cells

Burns may induce oxidative stress due to the increased production of reactive oxygen species (ROS) and/ or the promotion of cellular oxidation events. The effects of propofol, which plays an important role in antioxidant and organ protection, on burn serum-induced oxidative stress injury and its possible mechanisms were investigated in this study. Burn serum stimulation can lead to cell injuries in human dermal microvascular endothelial cells (HDMECs), including apoptotic cell death and increased cell permeability. Interestingly, these symptoms are alleviated in the presence of propofol. Furthermore, we found that the protective effect of propofol in heat stress-induced cell damage is closely related to its antioxidation. We further revealed that burn serum significantly reduces the level of SOD2 and SOD1 (P = 0.002), and propofol was only found to inhibit the reduction of SOD2. The transfection of HDMECs with SOD2 small interfering RNA (siRNA) markedly decreases the expression of SOD2, and the protective effect of propofol in siRNA SOD2 clones is significantly reduced. Taken together, these results indicate that propofol protects the burn serum-injured cells, at least partly through upregulating SOD2 expression to reduce the direct or indirect cell damage caused by oxidative stress.